Roles of ERK and NF-kappa B in Interleukin-8 Expression in Response to Heat Shock Protein 22 in Vascular Smooth Muscle Cells.
10.4196/kjpp.2008.12.4.171
- Author:
Seung Hun KANG
1
;
Ji Hyuk LEE
;
Kyung Ha CHOI
;
Byung Yong RHIM
;
Koanhoi KIM
Author Information
1. Department of Pharmacology, School of Medicine, Pusan National University, Busan, Korea. koanhoi@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Heat shock protein;
Interleukin-8;
Vascular smooth muscle cell
- MeSH:
Binding Sites;
Butadienes;
Cytoprotection;
Heat-Shock Proteins;
Hot Temperature;
I-kappa B Proteins;
Imidazoles;
Interleukin-8;
Molecular Chaperones;
Muscle, Smooth, Vascular;
Myocytes, Smooth Muscle;
NF-kappa B;
Nitriles;
p38 Mitogen-Activated Protein Kinases;
Promoter Regions, Genetic;
Protein Kinases;
Proteins;
Pyridines;
Shock;
Transcription Factor AP-1
- From:The Korean Journal of Physiology and Pharmacology
2008;12(4):171-176
- CountryRepublic of Korea
- Language:English
-
Abstract:
Heat shock proteins (HSPs) serve as molecular chaperones and play a role in cell protection from damage in response to stress stimuli. The aim of this article is to investigate whether HSP22 affects IL-8 expression in vascular smooth muscle cells (VSMCs), and which cellular factors are involved in the HSP-mediated IL-8 induction in that cell type in terms of mitogen activated protein kinase (MAPK) and transcription element. Exposure of aortic smooth muscle cells (AoSMCs) to HSP22 not only enhanced IL-8 release but also induced IL-8 transcript via promoter activation. HSP22 activated ERK and p38 MAPK in AoSMCs. HSP22-induced IL-8 release was inhibited by U0126, but not by SB202190. A mutation in the IL-8 promoter region at the binding site of NF-kappa B, but not AP-1 or C/EBP, impaired promoter activation in response to HSP22. Delivery of I kappa B, but not dominant negative c-Jun, lowered HSP22-induced IL-8 release from AoSMCs. These results suggest that HSP22 induces IL-8 in VSMCs via ERK1/2, and that transcription factor NF-kB may be required for the HSP22-induced IL-8 up-regulation.
